The influence of host genetics on erythrocytes and malaria infection: is there therapeutic potential?

Malaria Journal

Review

Brendan J McMorran¹  Simon J Foote¹  Patrick M Lelliott¹  Gaetan Burgio¹ 

[1] John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia;

关键词: Malaria;    Plasmodium;    Host;    Polymorphism;    Erythrocyte;    Red blood cell;    Invasion;    Growth;    Cytoadherence;    Phagocytosis;   

DOI  :  10.1186/s12936-015-0809-x

 received in 2015-02-25, accepted in 2015-07-15,  发布年份 2015

来源: Springer

【 摘 要 】

As parasites, Plasmodium species depend upon their host for survival. During the blood stage of their life-cycle parasites invade and reside within erythrocytes, commandeering host proteins and resources towards their own ends, and dramatically transforming the host cell. Parasites aptly avoid immune detection by minimizing the exposure of parasite proteins and removing themselves from circulation through cytoadherence. Erythrocytic disorders brought on by host genetic mutations can interfere with one or more of these processes, thereby providing a measure of protection against malaria to the host. This review summarizes recent findings regarding the mechanistic aspects of this protection, as mediated through the parasites interaction with abnormal erythrocytes. These novel findings include the reliance of the parasite on the host enzyme ferrochelatase, and the discovery of basigin and CD55 as obligate erythrocyte receptors for parasite invasion. The elucidation of these naturally occurring malaria resistance mechanisms is increasing the understanding of the host-parasite interaction, and as discussed below, is providing new insights into the development of therapies to prevent this disease.

【 授权许可】

CC BY   
© Lelliott et al. 2015